Bone Health in Pediatric Inflammatory Bowel Disease

Abstract

Children and adolescents with inflammatory bowel disease have multiple risk factors for impaired bone development, including poor growth, delayed maturation, malnutrition, decreased weight-bearing activity, chronic inflammation, genetic susceptibility, and immunosuppressive therapies, such as glucocorticoids. The impact can be immediate, such as fragility fractures in childhood or adolescence, or delayed, due to suboptimal peak bone mass accrual. Throughout childhood and adolescence, bone mineral accrual results in ethnic-, gender-, maturation-, and site-specific increases in bone dimensions and density. During the critical 2-year interval surrounding the time of peak height velocity, approximately 25% of skeletal mass is laid down and 90% of peak bone mass is established by 18 years of age. Dual energy x-ray absorptiometry (DXA) scans are widely accepted as a quantitative measurement technique for assessing skeletal status, and in children are expressed relative to age or body size as Z-scores. A three-dimensional structural analysis of trabecular architecture and cortical bone dimensions can be obtained by quantitative computed tomography. Children with newly diagnosed inflammatory bowel disease have deficits in bone mineral density, and longitudinal studies have demonstrated increased bone biomarkers and improvements in bone mineral density over time. Currently, the prevention of bone disease is best accomplished by controlling inflammation, providing adequate calcium and vitamin D supplementation, and encouraging physical activity. Prospective trials of therapeutic agents need to be performed to assess efficacy and safety in the developing skeleton.